Evaluation of daytime sleepiness and insomnia symptoms in OSA patients with a characterization of symptom-defined phenotypes and their involvement in depression comorbidity-a cross-sectional clinical study.

Introduction: Recent research highlights the significance of insomnia and sleepiness, shifting from obstructive sleep apnea (OSA) severity and sleep structure, in defining OSA phenotypes. Objectives: This study aimed to characterize insomnia and sleepiness associated with OSA phenotypes and assess their involvement in depression symptoms (DS) in OSA. Materials and methods: This cross-sectional, clinical study included 181 participants who underwent polysomnography (PSG) and filled out questionnaires, including the Epworth Sleepiness Scale (ESS), Insomnia Severity Index (ISI), Pittsburgh Sleep Quality Index (PSQI), and Beck Depression Index (BDI). They were categorized into phenotypes: insomnia-sleepiness (I + S; ESS ≥ 11; ISI ≥ 15; n = 20), sleepiness (S; ESS ≥ 11; ISI < 15; n = 22), insomnia (I; ESS < 11; ISI ≥ 15), and asymptomatic (A; ESS < 11; ISI<15; n=55). Results: A linear regression model for the BDI score (R2 = 0.357, p < 0.001) included ISI score and subjective-to-objective sleep latency ratio. The ISI score was a predictive factor for mild and moderate DS [OR = 1.23 (95% CI: 1.09-1.38), p < 0.001 and OR = 1.39 (95% CI: 1.13-1.72), p = 0.002]. The I and I + S phenotypes are characterized by higher BDI scores (p < 0.001 and p = 0.02), longer subjective sleep latency (p = 0.008 and p = 0.04), and shorter subjective total sleep time (TST; p = 0.049 and p = 0.006) compared to A. Furthermore, the I and I + S groups had shorter subjective TST than S (p = 0.03 and p = 0.047). The I and I + S had higher BDI scores than A (p < 0.001 and p = 0.02, respectively) and S (p < 0.001 and p = 0.02, respectively). The I phenotype was associated with the risk of mild and moderate DS (OR = 5.61 (95% CI: 1.91-16.53), p < 0.001 and OR = 9.55 (95% CI: 1.81-50.48), p = 0.008 respectively). Moreover, the I + S phenotype presented an even greater risk for mild DS (OR = 10.29 (95% CI: 2.95-35.85), p < 0.001). Conclusion: Using clinical features for OSA phenotyping holds promise for finding OSA individuals with increased risk for DS occurrence.

REM-OSA as a Tool to Understand Both the Architecture of Sleep and Pathogenesis of Sleep Apnea-Literature Review.

Sleep is a complex physiological state, which can be divided into the non-rapid eye movement (NREM) phase and the REM phase. Both have some unique features and functions. This difference is best visible in electroencephalography recordings, respiratory system activity, arousals, autonomic nervous system activity, or metabolism. Obstructive sleep apnea (OSA) is a common condition characterized by recurrent episodes of pauses in breathing during sleep caused by blockage of the upper airways. This common condition has multifactorial ethiopathogenesis (e.g., anatomical predisposition, sex, obesity, and age). Within this heterogenous syndrome, some distinctive phenotypes sharing similar clinical features can be recognized, one of them being REM sleep predominant OSA (REM-OSA). The aim of this review was to describe the pathomechanism of REM-OSA phenotype, its specific clinical presentation, and its consequences. Available data suggest that in this group of patients, the severity of specific cardiovascular and metabolic complications is increased. Due to the impact of apneas and hypopneas predominance during REM sleep, patients are more prone to develop hypertension or glucose metabolism impairment. Additionally, due to the specific function of REM sleep, which is predominantly fragmented in the REM-OSA, this group presents with decreased neurocognitive performance, reflected in memory deterioration, and mood changes including depression. REM-OSA clinical diagnosis and treatment can alleviate these outcomes, surpassing the traditional treatment and focusing on a more personalized approach, such as using longer therapy of continuous positive airway pressure or oral appliance use.